Extensive extrafacial granuloma faciale of the scalp

showed patches of macular depigmenlation (Fig. 2). A skin biopsy of an indurated lesion revealed a perivascular mononuclear inliltrate of the mid and deep dermis. with thickening of lhe deep dermis as assessed hy an elastin stain. Mucin stains were negative. Direct imnuinolluorcscence of lesional skin did not show specilic immune deposits. Additional laboratory investigatii)ns. including the erythrocyte sedimentation rate, red and while blood cell counts, a 25 parameter chemical analysis of serum, urinalysis including hydroxyproline excretion, serum electrophoresis. immunoelectrophoresis. antinuclear antibodies. anti-DNA. anti-RNP. anti-SM. antiRo autoantihodies. latex test. Clq binding test. CH50. C3, C4, a test for cryoglobulins. (C|-antitrypsin.T?.T4 were normal or negative. A chest X ray and an ophthalmologica! examination were normal. The patient was discharged on no treatment. The patient was .seen again in 1994. when she was well. All atrophic pigmented lesions had persisted hut the total number of skin lesions had not increased, hi place of the sclerotic plaques, atrophy of the superficial dermis and pigmentation was found. This patient had an inllammatory skin disorder which followed Blaschko's lines that evolved, either directly, or indirectly, via morphoca-Iikc lesions, into atrophy of the superlicial dennis with pigmentation. The patient can be considered to have morphoea occurring in HIaschko's lines if one accepts tliat atrophodcrma of I'ierini and Pasini is a variant of morphoea. as strongly supported by the study of Kent'ka vl al.'' However, most (brms of linear morphoea are thought to follow nerve segments. If one considers these to be separate entities one has to admit that some of the patient's lesions were not distinguishable from classical morphoea. It has been reported that some cases diagnosed as atrophoderma of Pierini and Pasini had sclerodermatous changes.'' As in morphoea. linear forms of atrophoderma of Picrini and Pasini are thought to be zosteriform.^ Linear atrophoderma of Moulin" is an acquired pigmented atrophy ofthe superficial dermis ordered in multiple bands that follow the lines of Blaschko. However, the live cases described by Moulin cf al.' and the case reported by Baumann cl iil.^ did not show inflammatory changes preceding the pigmentation and atrophy. Moreover, none of the skin lesions in these six patients, presented morphoea-like features, such as sclerosis and depigmentation. However, our patient s clinical presentation, 17 years alter the disease started, did not differ from the cases presented hy Moulin et al. As there are no biochemical or genetic markers available the relation between atrophoderma of Moulin and our case remains unclear. Nevertheless, our case clearly documents that acquired inllammatory processes in the dermis. with sclerodermatous and atrophic dermal sequelae, can follow the lines of Blasehko. Patients such as ours may help to identify the genes in the pathogenesis ofthe dilTuse or generalized counterparts